PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34454908-0 2022 Interaction of galectin-7 with HMGCS1 in vitro may facilitate cholesterol deposition in cultured keratinocytes. Cholesterol 62-73 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 31-37 34347016-3 2021 TDP-43 binds directly to mRNA of SREBF2, the master transcription regulator for cholesterol metabolism, and multiple mRNAs encoding proteins responsible for cholesterol biosynthesis and uptake, including HMGCR, HMGCS1, and LDLR. Cholesterol 157-168 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 211-217 34454908-6 2022 The amount of cholesterol, a final biosynthetic product of HMGCS1-involved pathway, was increased in Gal-7 treated cells, and was significantly reduced in Gal-7 siRNA transfected cells. Cholesterol 14-25 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 59-65 34454908-7 2022 The increase of cholesterol level in Gal-7 treated cells was inhibited by wild type HMGCS1 peptide but not by Phe-26 mutated peptide, suggesting that the interaction of Gal-7/HMGCS1 is related to cellular cholesterol level. Cholesterol 16-27 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 84-90 34454908-7 2022 The increase of cholesterol level in Gal-7 treated cells was inhibited by wild type HMGCS1 peptide but not by Phe-26 mutated peptide, suggesting that the interaction of Gal-7/HMGCS1 is related to cellular cholesterol level. Cholesterol 16-27 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 175-181 34454908-7 2022 The increase of cholesterol level in Gal-7 treated cells was inhibited by wild type HMGCS1 peptide but not by Phe-26 mutated peptide, suggesting that the interaction of Gal-7/HMGCS1 is related to cellular cholesterol level. Cholesterol 205-216 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 84-90 34454908-7 2022 The increase of cholesterol level in Gal-7 treated cells was inhibited by wild type HMGCS1 peptide but not by Phe-26 mutated peptide, suggesting that the interaction of Gal-7/HMGCS1 is related to cellular cholesterol level. Cholesterol 205-216 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 175-181 34454908-9 2022 These results are likely to indicate that Gal-7 induction in epidermal keratinocytes causes both apoptotic cell death and HMGCS1-mediated cholesterol accumulation which will be phagocytized by macrophages. Cholesterol 138-149 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 122-128 32523679-0 2020 KLF13 suppresses the proliferation and growth of colorectal cancer cells through transcriptionally inhibiting HMGCS1-mediated cholesterol biosynthesis. Cholesterol 126-137 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 110-116 35369058-9 2022 It was also observed that the occupancies of histone H3K27ac and H3K4me1, at the locus of the cholesterol metabolic genes HMGCR and HMGCS1, in the livers of PEDV-infected piglets, were suppressed. Cholesterol 94-105 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 132-138 33422461-5 2021 Microarray-based analyses indicated that interaction with ECs for 48 hours down-regulates expression of genes in VSMCs controlling rate-limiting steps of the cholesterol biosynthesis such as HMGCR, HMGCS1, DHCR24 and DHCR7. Cholesterol 158-169 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 198-204 33414447-6 2021 Meanwhile, MIEF2-promoted cholesterol biosynthesis through up-regulating the expression of sterol regulatory element binding protein 2 (SREBP2) and its transcriptional target cholesterol biosynthesis genes HMGCS1 and HMGCR. Cholesterol 26-37 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 206-212 33414447-6 2021 Meanwhile, MIEF2-promoted cholesterol biosynthesis through up-regulating the expression of sterol regulatory element binding protein 2 (SREBP2) and its transcriptional target cholesterol biosynthesis genes HMGCS1 and HMGCR. Cholesterol 175-186 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 206-212 34444698-5 2021 Consistent with the transcriptomic finding of down-regulated cholesterol metabolism, we demonstrated that both cholesterol contents and cholesterol biosynthesis/transformation gene expressions in the mycotoxin-exposed livers were reduced, including HMGCS1, FDPS, SQLE, EBP, FDFT1 and VLDLR. Cholesterol 61-72 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 249-255 34444698-5 2021 Consistent with the transcriptomic finding of down-regulated cholesterol metabolism, we demonstrated that both cholesterol contents and cholesterol biosynthesis/transformation gene expressions in the mycotoxin-exposed livers were reduced, including HMGCS1, FDPS, SQLE, EBP, FDFT1 and VLDLR. Cholesterol 136-147 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 249-255 35636243-6 2022 Further validation of three proteins, HMGCS1 (cholesterol synthesis), P4HA1 (glycolysis) and KDM5A (demethylation of histone 3 at lysine 4), confirmed their significant differential abundance, respectively. Cholesterol 46-57 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 38-44 35552960-1 2022 PURPOSE: In this study, we sought to explore the function of seven important enzymes (MSMO1, EBP, HMGCS1, IDI2, DHCR7, FDFT1, and SQLE) involved in cholesterol biosynthesis especially SQLE in PDAC therapy. Cholesterol 148-159 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 98-104 33601148-1 2021 Hydroxy-3-methylglutaryl-CoA synthase 1 (HMGCS1) is a key enzyme in the mevalonate pathway of cholesterol synthesis. Cholesterol 94-105 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 41-47 32523679-18 2020 Knockdown of HMGCS1 suppressed cholesterol biosynthesis and the proliferation of CRC cells with silenced KLF13. Cholesterol 31-42 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 13-19 32523679-20 2020 Conclusions: Our study reveals that KLF13 acts as a tumor suppressor in CRC through negatively regulating HMGCS1-mediated cholesterol biosynthesis. Cholesterol 122-133 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 106-112 26535009-4 2015 Expression of the ERBB4 ICD in mammary epithelial cells or activation of ERBB4 with the ligand neuregulin 1 (NRG1) induced the expression of SREBP target genes involved in cholesterol biosynthesis, including HMGCR and HMGCS1, and lipid uptake, LDLR, which encodes the LDL receptor. Cholesterol 172-183 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 218-224 28698273-2 2017 3-Hydroxy-3-methylglutaryl-coenzyme A (CoA) synthase 1 (HMGCS1), 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR [a rate-limiting step in the mevalonate pathway]), and farnesyl-diphosphate farnesyltransferase 1 (FDFT1 [a committed step in the cholesterol branch]) are repressed by multiple KSHV miRNAs. Cholesterol 243-254 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 56-62 32586423-9 2020 Furthermore, IGF1 upregulated the expression of cholesterol biosynthetic genes (3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), 3-hydroxy-3-methylglutaryl-CoA synthase (HMGCS1) and cytochrome P450, family 5, subfamily A, polypeptide 1 (CYP5A1)), but not sterol regulatory element-binding transcription factor 1 (SREBF1). Cholesterol 48-59 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 171-177 31528309-6 2019 Especially, HMGCS1 is the most central gene is also linked to one of the important colon cancer altered processes, cholesterol metabolism. Cholesterol 115-126 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 12-18 28972046-5 2017 Downregulation of cholesterol biosynthesis proteins, such as HMGCS1, occurred in PTEN-null cell lines and tumor xenografts sensitive to AZD8186. Cholesterol 18-29 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 61-67 15213220-3 2004 Among them, a cluster of genes involved in fatty acid and cholesterol biosynthesis, including stearoyl-CoA desaturase (SCD), fatty acid synthase, and hydroxymethylglutaryl-CoA synthase (HMGCS), was up-regulated by PDGF after 24 h of treatment, and their expression correlated with increased membrane lipid production. Cholesterol 58-69 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 150-184 25933205-2 2015 Here, we demonstrate that the 5-aminoimidazole-4-carboxyamide ribonucleoside (AICAR)-induced activation of AMPK directly inhibited the expression of SREBP-2 and its target genes HMGCR and HMGCS, which are key enzymes in cholesterol biosynthesis, and suppressed the TSH-stimulated up-regulation of SREBP-2 in HepG2 cells; similar results were obtained in TSH receptor knockout mice. Cholesterol 220-231 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 188-193 24711211-6 2015 Real-time RT-PCR showed that GDF9 increased messenger RNA (mRNA) levels of enzymes required for cholesterol biosynthesis, such as 3-hydroxy-3-methylglutanyl-CoA synthase 1 (HMGCS1), farnesyl-diphosphate farnesyltransferase 1, squalene epoxidase, lanosterol synthase, and cytochrome P450, family 51, subfamily A, polypeptide 1 (CYP51A1). Cholesterol 96-107 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 130-171 24711211-6 2015 Real-time RT-PCR showed that GDF9 increased messenger RNA (mRNA) levels of enzymes required for cholesterol biosynthesis, such as 3-hydroxy-3-methylglutanyl-CoA synthase 1 (HMGCS1), farnesyl-diphosphate farnesyltransferase 1, squalene epoxidase, lanosterol synthase, and cytochrome P450, family 51, subfamily A, polypeptide 1 (CYP51A1). Cholesterol 96-107 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 173-179 18499393-7 2008 Up-regulated proteins were Glyoxalase-I (Glo 1) and 3-Hydroxy-3-methylglutaryl-Coenzyme A synthase 1 (HMGCS1) in cells with PL shown by TEM (favouring the cholesterol biosynthesis increase hypothesis for citalopram induced PL). Cholesterol 155-166 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 52-100 18499393-7 2008 Up-regulated proteins were Glyoxalase-I (Glo 1) and 3-Hydroxy-3-methylglutaryl-Coenzyme A synthase 1 (HMGCS1) in cells with PL shown by TEM (favouring the cholesterol biosynthesis increase hypothesis for citalopram induced PL). Cholesterol 155-166 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 102-108 24170205-5 2013 In the current study we aimed to establish whether the expression of genes encoding enzymes related to cholesterol (hmgcs1, hmgcr, fdft) and fatty acid biosynthesis and LDL receptor can be induced by an iso-physiological copper concentration. Cholesterol 103-114 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 116-122 20162334-3 2010 Whole genome gene profiling using DNA chip technology revealed that genes involved in cholesterol and fatty acid metabolism (low-density lipoprotein receptor, LDL-R; 3-hydroxy-3-methylglutaryl-Coenzyme A synthase 1 (HMGCS1) and fatty acid desaturase 1 (FADS1) are up-regulated after exposure of vascular smooth muscle cells with soluble ferrous iron. Cholesterol 86-97 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 216-222 19088433-8 2008 In conclusion, we provide evidence that ACBP is a transcriptional regulator of the HMGCS1 and HMGCR genes encoding rate-limiting enzymes of cholesterol synthesis pathway. Cholesterol 140-151 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 83-89 15213220-3 2004 Among them, a cluster of genes involved in fatty acid and cholesterol biosynthesis, including stearoyl-CoA desaturase (SCD), fatty acid synthase, and hydroxymethylglutaryl-CoA synthase (HMGCS), was up-regulated by PDGF after 24 h of treatment, and their expression correlated with increased membrane lipid production. Cholesterol 58-69 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 186-191